Monday, March 5, 2018

CDT Vaccines

CDT vaccines are commonly accepted as being necessary annually to keep goats healthy. Clostridial bacteria are found in the soil, and the clostridial diseases can cause sudden death. CDT vaccines protect goats from these diseases.
Two vaccines are commonly used for goats, a 3-way vaccine called CDT and an 8-way vaccine called Covexine-8. The 3-way vaccine protects goats from clostridium perfringins type C and D (overeating disease) and clostridium tetani (tetanus). The 8-way vaccine protects goats against additional forms of clostridium, but the 3-way vaccine is usually sufficient for dairy goats in the US.
The tetanus toxoid in the 3-way vaccine provides long term protection from tetanus (deadly if untreated) which is caused when a wound becomes infected with tetanus bacteria.
Enterotoxemia is a condition where the clostridium bacteria normally present in a goat’s intestinal tract grow uncontrollably. This occurs when the movement of food through the intestines slows because of overeating of grain, spring pasture, milk or milk replacer. It often occurs after goats eat too much spring growth, and is therefore commonly referred to as “overeating” disease (also deadly if untreated).

WHEN TO VACCINATE GOATS WITH CDT

Does, bucks and wethers should receive CDT shots annually, and it’s common for breeders to give pregnant does their annual shot about a month before they’re due to freshen. This passes immunity to the kids when they drink the colostrum of the dam. 
The kids immunity will begin to decline at about six weeks, so it’s common for breeders to give kids their first CDT vaccine at six to eight weeks, followed by a booster three to four weeks later. If kids are from a dam that has not been vaccinated, they can be vaccinated at three to four weeks, and also need the booster three to four weeks lateaccinating kids born to unvaccinated dams earlier may not be effective due to their immature immune system. If kids from unvaccinated dams are going to be disbudded or castrated before immunity can be established, then the tetanus antitoxin should be used to provide temporary, short-term protection from tetanus. They will still need to be vaccinated with the CDT toxoid at three to four weeks, and again in three to four weeks to establish long-term protection for all three diseases.
HOW TO GIVE CDT VACCINATIONS
CDT injections are given subcutaneously (SQ or subQ) under the skin. A needle length of about 1”, gauge of 18 to 20, and the “tent” method is used. The loose skin is pulled up in the area of the injection site. The syringe and needle are held parallel to the body and the needle is pushed through the skin to administer the vaccine into the cavity created.
The dosage for CDT is 2ml for adults or kids. It’s not uncommon for an abscess to develop at a CDT injection site, so the armpit (region behind the base of the front legs) is often the preferred site for CDT vaccinations. Always use a new needle to vaccinate each goat. CDT vaccines should be stored in the refrigerator.

Sunday, December 17, 2017

Learning About The Doe Heat Cycle For New Goat Owners

It’s a fact about goats that some females, or does, experience heat cycles year around. Others come into heat only during the fall months. Throughout the breeding season, a doe periodically comes into heat or estrus.  

During the peak of estrus, known as standing heat, a doe is receptive to a buck’s attention and can become pregnant. This phase of the reproductive cycle may last between 12 to 36 hours.

The time between the start of one estrus and the start of the next is called the estrous cycle. Different individual does have different estrous cycles. A doe’s cycle can range anywhere from 18 to 24 days, with 21 days being typical. Keeping track of the length of each of your doe’s cycles is a valuable breeding aid.

The female goat is called a “doe” or “nanny.” Up to the age of 12 months, she is sometimes referred to as a “doeling.” The doe can reach puberty between 4 to 12 months of age, depending on the breed, season of birth, level of feeding/nutrition, and overall health status. 

Under-feeding can lower her chances of getting pregnant and having kids and can also reduce milk production after having kids.The genetic makeup of the animal also determines when puberty occurs in the female. Puberty is reached when the female exhibits her first heat (estrus) and ovulation. 

The gestation period, or length of pregnancy, of the doe ranges between 145 to 152 days, or 150 days (5 months) on average, and under normal circumstances, the doe can have multiple births.

Signs of doe being in heat ( may only show a few)

  1. Constantly seeking attention
  2. General attitude change   
  3. Nervousness    
  4. Mounting other goats                                                   
  5.  Doe gets talkative/bleating                                          
  6. Her tail gets sticky                                              
  7. Doe urinates often                                                           
  8. Swollen Pink Vulva                                                         
  9. Mucus discharge from the vulva                            
  10. Tail "Flagging"                                                          
  11. Standing to be mounted                                          
  12. Fighting/headbutting others                                  
  13. Stands by buck pen                                                       
  14. Pacing down the fence line 


Note...Your doe may desperately try to get to the buck if there is one nearby. She may also be unusually uneasy OR abnormally affectionate (depends on the goat). If your goat doesn't show any of these signs above, it's called a silent heat.

The Buck

Male goats (called bucks) can breed pretty much any time. ... They'll only breed when they can smell that the female is in “heat”. Bucks can go into a “rut” which basically means they get a surge of hormones and ready to breed before a doe is ready.
They urinate all over themselves and will be covered from head to toe and be sticky, stinky, and slimy.

While in rut the buck will do a lot of tongue waving, blubbering, spitting, stomping and singing the wonderful song "wup", "wup", "wup". He will drink or sniff the does urine if given the chance then raise his lip and curl it back and make the funny“buck face” smelling the air all around him. the lip curl is called the Flehman response.

Keep in mind Bucks can and will breed through a fence if given the chance. 

Sunday, November 12, 2017

G6S - What is it and why do we care?

A Genetic Defect and its Management
By Dagny Vidinish
All animals, including dairy goats, have numerous genetic defects of varying severity. We are all familiar with the occasional multiple teats, for instance, and with such defects as undershot and overshot jaws. Other defects are rapidly fatal, and it often is unclear whether the death of a kid should be attributed to genetics or to misfortune. The exact inheritance of many of these defects is often obscure; for instance, although most people believe that multiple teats show up when both parents carry a gene for this trait there is evidence that in some cases they are actually caused by environmental factors. In order to manage these undesirable genes breeders usually have to fall back on the "don't repeat that breeding" strategy, which is very crude and unsatisfactory. 
This article will describe a recently discovered genetic defect which is easily managed and eliminated because its mode of  transmission is straightforward and, more important, because a foolproof DNA test is available to identify carriers of the gene.
This defect's full names are mucopolysaccharidosis IIID, or G-6-Sulfase deficiency, and it is usually referred to as G-6-S. It was first identified in 1987 at Michigan State University, and subsequently the researchers tested nearly one thousand goats in Michigan and concluded that about 25% of Nubians carry this gene. All cases are the result of a single mutation, and appear to be confined to Nubians and their crosses; other breeds were tested initially and they do not have this particular defect.
The affected goats lack an enzyme (G-6-S) and this results in a variety of symptoms of varying severity. The main symptom exhibited by affected goats is failure to grow. Sometimes the kid is smaller than normal at birth, and  grows slowly. Some breeders have reported kids which grew normally for the first three months and then stopped growing. Other affected goats grow to what appears to be normal size but is in fact small for the particular bloodlines. They lack muscle mass, appear "slab-sided", sometimes with blocky heads. Immune function appears to be compromised, and sometimes they become deaf or blind. The longest-lived goat known to be G-6-S affected died at just under four years of age, and death is usually due to heart failure. Unfortunately affected animals can and do grow up to breed, although they often experience reproductive problems.
The same symptoms can have many other causes, so that affected animals are seldom recognized as having a genetic defect. Often they grow normally for the first few months and may be sold before any problems become apparent. In that case the breeder may blame the new owner for the goat's failure to thrive and early demise.
Every animal has two genes for every trait, one inherited from the dam and one from the sire. In turn, that animal will pass only one of those genes to each offspring, and which one it will be is a matter of chance, like the flip of a coin. On the average, half the offspring will inherit one gene and half the other. If the two genes are different, then there is a question as to which of them will determine how the animal actually looks or functions. The defective G-6-S mutation is a simple recessive gene, which means that a goat which has only one copy of it will appear perfectly normal and will not show any of the symptoms described above. Such a goat is referred to as a "carrier". A goat which inherits the defective gene from both parents shows symptoms and is referred to as "affected". A "normal" goat, in this context, is one who has two copies of the normal gene.
If a normal goat is bred to a carrier, then all offspring will inherit a normal gene from the normal parent. The carrier parent will pass a normal gene to half the offspring, and a defective gene to the other half. Thus such a mating will, on the average, produce half normal kids and half carriers, and no affected ones. If two carriers are bred to each other, then one quarter of the kids will be normal, one half will be carriers, and one quarter will be affected. If an affected goat is bred to a normal goat, all offspring will be carriers. An affected goat bred to a carrier will produce half carriers and half affected.
As stated above, research shows that 25% of Nubians carry the defective G-6-S gene. Almost all of these are carriers, since most of the affected animals which are born would be culled, and the rest die early. Most people find it surprising that something which is in one quarter of the population can have escaped notice for so long. However, random matings in such a population would result in only one out of sixteen being carrier to carrier, and only one quarter of the kids from these breedings would be affected. Thus only one kid in sixty-four (1.6%) would be affected. Given the variable and obscure symptoms of G-6-S affected kids, it really is understandable that most Nubian breeders believe that they have never encountered affected kids.
However, many Nubians are line-bred, and this practice will concentrate certain genes in some lines while eliminating them from others. It has been observed that the G-6-S mutation is very prevalent in the same lines which are known for high milk production. Thus breeders who have been selecting for milk may have inadvertently also been selecting for the G-6-S defect. Fortunately it appears that the two traits are actually independent, that you can cull the G-6-S carriers without at the same time culling the high producers.
Usually it is difficult to eliminate a genetic defect without losing all the good genetics for which a line is known. For instance, if a buck throws double teats, then there is no way of knowing which of his offspring will do the same and which will not. You can cull him, but that seems rather heavy-handed since the bad gene will undoubtedly live on in some of his relatives. With G-6-S we are very fortunate to have a foolproof DNA test available which will tell us whether a goat is normal, or a carrier, or affected. This test makes it possible to save the good genetics and eliminate the defective gene if that is our wish. If a superior animal is a carrier, then we can test the kids and manage them in such a way as to avoid the birth of any affected individuals.
What is a good management strategy? What is the most efficient way to save the good and get rid of the bad? The usual recommendation for such testable defects is to cull carrier males, but not the females. Remember that if a normal buck breeds a carrier doe, then only half the kids will be carriers, and none will be affected. Thus if there are some carrier females in the herd, then using only normal bucks will reduce the incidence of carriers in the next generation by one half. The average herd would start with 25% carrier females, and if only normal bucks were used the next generation of females would be down to 12.5% carriers, and the next generation to 6.25%, etc. This is in sharp contrast to what a carrier buck would do in the same herd: if used to breed all the does, his daughters would be 50% carriers and 6.25% affected. Clearly there is much to be gained by testing buck kids and retaining only normal ones for breeding.
While it is relatively easy to cull a buck kid, one might hesitate to do the same with a proven sire. In particular, there are some very popular bucks whose semen commands a high price and who are carriers for the defective G-6-S gene. A reasonable strategy here would be to use these bucks only on normal does, thus avoiding affected kids. Then one would test the kids and cull carrier bucks.
Although the DNA tests are expensive, if testing one's bucks prevents the birth of even one affected kid then it is cost effective. Unlike tests for diseases, a genetic test does not need to ever be repeated. Also, the DNA tests are completely accurate, there are none of the gray areas which can be so frustrating. There is no need to test the kids if both parents are known to be normal. One can work back from one's foundation animals and if there really is no problem in the herd then it may be possible to establish that at reasonable cost. Normally whole blood is used for the test, but semen can also be used. If an AI buck is a carrier, that can be established by finding a carrier offspring out of a normal doe, but no number of normal offspring will prove that a buck is nomal.
A number of breeders have expressed the opinion that the G-6-S defect is no more of a problem than many other genetic defects, and therefore does not merit any particular attention. They evidently miss the point that it is the availability of a DNA test which makes this defect special. One can use goats from bloodlines which are known to have a high concentration of the G-6-S defect completely safely by just testing the particular individuals and either rejecting carriers or using them with proper precautions. There is nothing to be gained by trying to sweep G-6-S under a rug, and much to be gained by sharing information about it.
One may wonder why a DNA test has been developed for such an obscure defect, and no help is available for, say, multiple teats. The answer is simple - humans don't have a problem with multiple teats, they do with G-6-S. The same genetic defect, when found in humans, is called Sanfilippo IIID; the affected child appears normal at birth but soon stops growing, looses muscle mass, has neurological deterioration and dies. When the same genetic defect was discovered in goats researchers used them as models for treatment, and goat breeders in turn benefited from their discoveries.
Faith is the substance of things hoped for, the evidence of things not seen. ~Hebrews 11:1